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Goal Oriented Therapy after

Congenital Heart Surgery


or
What’s with this Venous Blood
Gas Stuff?
Anthony Rossi, MD
Director, Cardiac Intensive Care Program
Miami Children’s Hospital
Miami, FL USA
Background
• Monitoring oxygen delivery in the critically ill
pts after congenital heart surgery and
developing treatment plans to optimize
oxygen delivery , is a logical approach to pt
management and has been shown to improve
outcome in a wide spectrum of critical illness
• Critically ill pts achieving a normal or
supernormal level of oxygen delivery have
lower mortality, less end organ damage,
lower morbidity and shorter hospital stays
Oxygen Delivery=DO2
• DO2=Cardiac Index x Arterial Oxygen
Content (CaO2)
Indirect Indicators of Systemic DO2

• pH
• HCO3
• BE
• SVO2 (AVO2, OER)
• CO2 (SvCO2-SaCO2)
• lactate
Common Cardiac Surgical
Procedures
• Arterial switch operation
• Repair of tetralogy of Fallot
• VSD closure
• ASD closure
• AVC repair
• Rastelli operation
• Norwood operation
• Bi-Glenn
• Fontan
• Repair IAA
• BTS
• Central shunt
• Ross
• MV replacement
• AV replacement
• Aortic Valvotomy
• Konno
• Ross-Konno
• Repair TAPVC
• Repair coarctation
• Repair DORV
• Senning
• Mustard
• Double switch
Single Goal of PO Care

• Maintain optimal tissue oxygen delivery


Goal of Post-Op Care
• Maintain Optimal Tissue Oxygenation
– global
– regional
• splanchnic - the correction of
unrecognized perfusion defects seems
to be a desirable addition to the
standard clinical management of
critically ill patients with regard to
preservation of organ function*
• coronary
* J.-L. Vincent. Intensive Care Med (1996) 22:3
Determinants of Tissue
Oxygenation
• C.O.
• Hb
• SaO2
• O2 Demands (oxygen consumption: VO2)
Hemodynamic Monitoring: All mechanisms of
hemodynamic monitoring are used to estimate the
relationship of oxygen delivery to oxygen consumption. This
relationship might be considered an indicator of
cardiovascular well-being. Traditional hemodynamic
parameters include:
• HR, BP, central filling pressures
• perfusion
– cap refill
– extremity temp
• urine output
• arterial blood gas (pH, bicarb, BE)
• blood lactate
Systemic Venous Oxygen Saturation
(SvO2) Monitoring:

• defines the relationship of DO2/VO2


• estimate oxygen delivery (AVO2
difference, OER: oxygen extraction
ratio)
• estimate cardiac output trends
• estimate Qp/Qs in single ventricle pts
– SaO2 poor indicator of Qp/Qs (low SvO2
will decrease SaO2 in face of large Qp/Qs)
Causes of Low SVO2
• SVO2 = SaO2 – (VO2/Q x Hb x 13)
1 2 3 4

1 – Hypoxemia
2 – Increased metabolic rate
3
– Low cardiac output
4 – anemia
OER: Oxygen Extraction Ratio
• OER = O2 consumption/O2 delivery
• OER = O2 Sat art - O2 Sat sys ven
O2 Sat art
• normal relationship of 5/1 DO2/VO2
• normal OER = 0.2
• Omega is the reciprocal of the OER (normal value is
5)
• higher omega and lower OER are associated with an
improved relationship of DO2 to VO2.
Relation of DO2 to VO2: Under normal conditions, the cardiovascular
system delivers approximately 5 times as much oxygen as the body uses.
This would be reflected by an SvO2 of 80%, an A-VO2 difference of 20 or an
oxygen extraction ratio (OER) of 0.2. As oxygen delivery (DO2) decreases,
SvO2 decreases, the A-VO2 difference increases and the OER increases.
Oxygen consumption (VO2) should not be affected by DO2. At the critical
point of DO2, further decreases in DO2 are associated with a pathologic
decrease in VO2. This pathologic relationship is associated with increased
lactate production.
*
0.5 0.2 OER

VO2
critical point of DO2
(VO2 , lactate )

DO2
* Decreasing CV Reserve
Relation of DO2 to VO2: The graph now shows how decreasing cardiac
output (or more appropriately DO2) is associated with an SvO2 which drops
from 80 to 50 while the AVO2 difference increases from 20 to 50. This
graphic demonstration of the pathologic relationship of VO2 to DO2 will look
somewhat different under various pathologic conditions, such as sepsis.
The principles are similar however. Also, remember that the SvO2 is the
sum of all systemic venous return. Lactate elevation does not correlate
precisely with SVO2.
*
SVO2=50 SVO2=80
AVO2=50 AVO2=20
VO2
critical point of DO2
(VO2 , lactate )

Bad CO Excellent CO
* Decreasing CV Reserve
AVO2 difference vs. OER

• AVO2 diff of 25 in pt with SaO2 100%


– OER = 25/100 = 0.25
– DO2/VO2 = 4/1 (normal)
• AVO2 diff of 25 in pt with SaO2 65%
– OER = 25/65 = 0.38
– DO2/VO2 = 2.5/1 (2/1 = critical point of DO2!)
– This pt is living on the edge!
OER in Infants following Heart Surgery: This study showed that in infants
undergoing congenital heart surgery, survivors and nonsurvivors had similar
OER, or indices of cardiovascular well-being, on admission to the CICU and
at 24 hrs after admission. At 6 hours after admission, nonsurvivors showed a
severe derangement in the DO2/VO2 (either decreased DO2 or increased
VO2). It was presumed that the oxygen debt in these patients was so great
at 6 hours, that improvement in DO2 thereafter was not associated with
survival. 0.6
0.5
*
0.4
Survivors
OER

0.3
Non Survivors
0.2
0.1
0
Admit 6 hours 12 18 24
hours hours hours
time after admission to CICU
Rossi, Seiden, Gross, et al. Annals Thorac Surg. 1999
-15 -10 -5 0 5 10 15
Base Excess

Base Excess vs Blood Lactate


elevated lactate
- base excess elevated lactate
+ base excess
lactate

10

2.2
normal lactate normal lactate
- base excess r2 = 0.27 + base excess
-10 -5 5 10
Base excess
The base excess does not predict blood lactate levels. Pts with a positive
base excess can have severe hyperlactatemia.
Lactate Monitoring after CHS: A number of studies have shown
the predictive value of blood lactate levels after CHS.

Children after cardiac surgery


Initial lactate > 4.2 mmol/l - mortality 100%
(Siegel et al.1996)
Initial lactate > 4.5 mmol/l - mortality 79%
(Hatherhill et al.1997)
Infants after cardiac surgery
• Initial lactate > 7mmol/l - mortality 55%
• Maximum lactate > 9mmol/l - mortality 86% (Chefitz et al. 1997)
Serial Lactate Measurements Predict Outcomes after CHS
Charpie et al. 2000
Speculation: In the summer of 2001, the cardiac surgical
program began to wonder…..

• If lactate is useful in predicting outcomes in pts after


CHS could lactate be used as a target goal for medical
management in this pt population?
• Can GDT be applied to pts after CHS?
July 2001: The Premise
• Establish near patient testing of routine critical care lab values
with rapid turn-around-time
– Clinician can react quickly to changing physiologic conditions
• Establish blood lactate measurement as objective indicator of
oxygen debt
• Establish clinical guidelines which are directed at normalizing
blood lactate levels (thereby minimizing oxygen debt)
• The combination of the above would increase survival after
congenital heart surgery
Lactate Management Protocol
Initial Lactate > 2.2
Repeat q4hrs x 4

No Change Increase in Lactate Decrease in Lactate

<5 >5 Escalate Medical Rx Repeat Q 4 Hrs

Repeat in 4 hrs Escalate Medical Rx Repeat in 4 hrs

Repeat in 4 hrs Lactate > 10

Lactate < 5 Lactate 5-10 Consider CPS

Repeat in 4 hrs Escalate Medical Rx

CPS = Cardiopulmonary Support


MCH Goal Directed Lactate
Management Strategy in
Postoperative Patients

Lactate Normal
or No Changes
Diminishing
MCH Goal Directed Lactate
Management Strategy in
Postoperative Patients
pH normal?

pCO2 appropriate?

Lactate Elevated Hb appropriate?


Or
CVP appropriate?
Rising
HR appropriate?
BP appropriate?

Increase Oxygen Delivery


Patients Undergoing CHS at
MCH from 6/95-12/07
ERA Age Weight Total < 1 mth > 1 mth
(Range) (Range) Pts
Median Median

6/95- (0-72 yrs) (0.5-127 kg)


6/01 311 d 7.9 kg 1656 321 1335

7/01-
(0-72 yrs) (0.4-114 kg)
12/07 1810 445 1365
166 d 5.8 kg
P < 0.01 P < 0.01

Adapted and updated from: Point of Care Testing and Goal Directed Therapy
Improve Outcomes after Congenital Heart Surgery. Rossi et al. Intensive
Care Med. 2005
Total Oxygen Debt is Related to Outcome: The concept of “lactime” was
described by Bakker and colleagues in 1999. The peak lactate alone may
not be the best predictor of mortality in critical illness, the total area under the
curve that one spends with an elevated lactate, or in oxygen debt, may be a
better predictor.

12
10
8
lactate

Pt 1
6
Pt 2
4
2
0

admit 6 hrs 12 18 24
hrs hrs hrs

“lactime” Bakker, Am J Surg 1996


In a study of lactate patterns of children after congenital heart surgery, peak
lactate level correlated with mortality. Interestingly, earlier studies of critically ill
adults in surgical ICUs showed that mortality was almost 100% in that
population if the blood lactate level was above 10. These children routinely
survived with lactate levels above 10 and occasionally survived with lactate
levels greater than 20. Unpublished data from the Mt. Sinai Medical Center.

80
66.7
70
60
% mortality

50 44.4
40
30
20 11.5
10 1.6
0
<5 5-10 10-20 > 20
peak lactate
Lactate on admission to the CICU and peak lactate correlated with
outcome in our study. The time it took to reach the peak lactate
level was also higher in nonsurvivors. So pts who die not only have
higher levels of lactate but also take longer to peak and spend more
time in “oxygen debt.”
18
16 15.3
N=41
14
blood lactate or time in hours

P<0.001 P<0.001
12
9.9
10
8.4 8.1
8 6.7
6
4 3.1
2
0
Admission lactate Peak lactate (mmol/l) Time to peak lactate
(mmol/l) (hours)
NONSURVIVORS SURVIVORS
Lactate Monitoring in Pts Who Survive: Individual pts who survive congenital
heart surgery can have differing lactate curves. Pt number 1 is admitted after a
high risk operation with a markedly elevated lactate that returns to baseline fairly
rapidly with aggressive medical therapy. Pt 2 has a more delayed response to
medical therapy but ultmately improves the DO2/VO2 relationship and survives.

Low risk cardaic pts exhibit only mild elevations in blood lactate (pt 3).
10
9 9
8
7 7
6 PT1
5 5 5 5 PT2
4 4 4 4 PT3
3 3 3
2 2 2 2 2
1.5
1
0
ADMIT 6 HR 12 HR 18 HR 24 HR
Category 1-4 Survivors (excluding CPS patients)
n=127
10 Category 1 Mean
Category 2 Mean
8
Category 3 Mean
lactate(mmol/L)

6 Category 4 Mean

0
0 10 20 30 40 50
hours postop

Patterns of Lactate Values after Congenital Heart Surgery and Timing of Cardiopulmonary
Support. Robert L. Hannan, MD * , Marion A. Ybarra, BS, Jeffrey A. White, MS, Jorge W. Ojito,
CCP, Anthony F. Rossi, MD, Redmond P. Burke, MD Ann Thorac Surg 2005;80:1468-1474
Category 1-4 Survivors (excluding CPS patients)

10
n=127

8
lactat (mmol/L)

4 y = 4E-05x 3 - 0.0018x 2 - 0.0197x + 2.5738

0
0 10 20 30 40 50
hours postop

Patterns of Lactate Values after Congenital Heart Surgery and Timing of Cardiopulmonary Support.
Robert L. Hannan, MD * , Marion A. Ybarra, BS, Jeffrey A. White, MS, Jorge W. Ojito, CCP, Anthony
F. Rossi, MD, Redmond P. Burke, MD Ann Thorac Surg 2005;80:1468-1474
Survivors Excluding CPS Patients
8

7 Category 1-4
Category 6
6
lactate (mmol/L)

5 3 2
y = 0.0002x - 0.0176x + 0.3418x + 3.0448
4

1 3 2
y = 4E-05x - 0.0018x - 0.0197x + 2.5738
0
0 10 20 30 40 50
hours postop

Patterns of Lactate Values after Congenital Heart Surgery and Timing of Cardiopulmonary Support.
Robert L. Hannan, MD * , Marion A. Ybarra, BS, Jeffrey A. White, MS, Jorge W. Ojito, CCP, Anthony F.
Rossi, MD, Redmond P. Burke, MD Ann Thorac Surg 2005;80:1468-1474
Non Survivors (excluding CPS Patients)
20
18
16
14
lactate (mmol/L)

12
10
8
6
4
2
0
0 10 20 30 40 50
hours postop
Patterns of Lactate Values after Congenital Heart Surgery and Timing of Cardiopulmonary Support. Robert
L. Hannan, MD * , Marion A. Ybarra, BS, Jeffrey A. White, MS, Jorge W. Ojito, CCP, Anthony F. Rossi, MD,
Redmond P. Burke, MD Ann Thorac Surg 2005;80:1468-1474
Lactate Monitoring in Pts Who Die: Pt 1 exhibits a typical lactate pattern of a pt
who dies after congenital heart surgery. The lactate on admission is high and
despite attempts to improve the DO2/VO2 relation, lactate continues to rise.
Rarely, a pt will be admitted after surgery with a low lactate that rises despite
therapy and dies. Some pts may “honeymoon” and show deterioration later
(pt 3). Serial lactate monitoring is valuable even in pts who are admitted and
appear clinically well.
14

12 12
11
10 11 11 10
8 8 PT 1
PT 2
6 7 7
6 PT 3
4 5
4
2 3 3
2 2
0
ADMIT 6 HR 12 HR 18 HR 24 HR
Venous Blood Gas Monitoring
• VBG monitoring allows you to calculate the a-vCO2
(the difference b/w the arterial and venous pCO2) and
a-vpH (the difference b/w the arterial and venous pH)
gradients in the critically ill
• a-vCO2 is directly related to Cardiac Output
– This difference, also known as the CO2 GAP, is a better
indicator of cardiac output than the a-vO2 difference
• The larger the a-vCO2 gradient, the lower the cardiac
output
• pH gradient has been used to access pts in shock
Effect of Cardiac Output on
vCO2
aCO2=40 aCO2=40

CO2 CO2
CELL CELL

Normal CO Low CO

vCO2=45 vCO2=52
AVCO2, AV pH, Lactate and
OER in Survivors After Heart
Surgery
9 0.45
8
0.4 lactate
AVCO2, AVpH, Lactate

7
6 0.35 AVCO2

OER
5 0.3 AVpH
4 OER
0.25
3
2 0.2
admit 6 hours 12 hours 18 hours 24 hours
Objective Indicators of DO2 in Varying
Physiologic States
VpH SvO2 AVO2 O2 EF OER AVCO2 Lactate

Normal CO <0.05 75% 25% 4 0.25 <7 <2.2

Decreased >0.05 66% 33% 3 0.33 8-12 <2.2


CO

Critical >0.05 50% 50% 2 0.50 >12 >2.2


Point of
DO2
VBG/ABG
VBG ABG A-V pH/
pH/CO2/SvO2 pH/CO2/SaO2 A-V CO2/
A-V O2

Normal 7.35/45/75 7.40/40/100 0.05/5/25

Resp 7.20/70/65 7.25/65/90 0.05/5/25


Acidosis
Low CO 7.15/70/50 7.30/40/100 0.15/30/50
Conclusions
• Optimizing DO2 is a goal oriented task and it’s rewards are
rapidly appreciated.
• Goal oriented medical therapy may be directed at a number of
objective parameters after congenital heart surgery, but SvO2
and blood lactate have shown the most promise.
• SvO2 and Lactate monitoring are complimentary techniques to
evaluate cardiovascular well-being.
• The currently available technologies allow SvO2 monitoring to
occur continuously and in real-time. Lactate monitoring is
intermittent.
• Small victories are critical in the psyche of all involved in the
care of the most critically ill.
• Objective indicators of cardiovascular well-being must be
accurate, reproducible and available rapidly to be useful.
Conclusions
• VBG (a-vCO2 and a-vpH) and SvO2 allow the clinician to rapidly assess
if a new treatment is having it’s desired effect (increasing DO2 or
improving DO2 / VO2).
• SvO2 monitoring has been proven to save the lives of critically ill pts.
• The highest risk pts, such as those who undergo the Norwood operation
seem to benefit most.
• Lactate monitoring tells the clinician how well the patient has been doing
over an extended period of time, it is evidence of end-organ injury.
• Blood lactate levels can change very rapidly with changes in DO2/VO2.
Lactate levels do not show significant “lag-times.” Lactate wash-out as
a cause of persistently elevated lactate levels probably does not occur
frequently in the critically ill. A more likely reason for persistence of an
elevated lactate is continued tissue hypoxia. If the lactate remains high,
the patient is not better!
• Increase in blood lactate does not necessarily mean tissue oxygenation
is poor (inability to metabolize lactate appropriately occurs in liver
failure), however, whatever the cause of hyperlactatemia, it is always
associated with increased morbidity and mortality.
Who’s Minding the Store?
• Subjective indicators of cardiovascular well-being
must be complemented by objective indicators
• Objective indicators are necessary since the level of
experience of the person responsible for the care of
the critically ill patient after heart surgery varies
significantly, even within ICUs.
• It has been show that even experienced clinicians
can misjudge a pts overall cardiovascular well-being
(blood lactate level or SvO2).
• Objective indicators must be accurate, reproducible
and available rapidly to be useful.